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Tytuł pozycji:

Brain-computer interface controlled robotic gait orthosis

Tytuł :
Brain-computer interface controlled robotic gait orthosis
Index Terms :
Life Sciences
Medicine and Health Sciences
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride: pharmacology
Animals
Cats
Dimethylphenylpiperazinium Iodide: pharmacology
Electric Stimulation
Enkephalin
Leucine: pharmacology
Methionine: analogs & derivatives; pharmacology
Enkephalins: pharmacology; physiology
Female
Ganglia
Sympathetic: drug effects; physiology
Heart Rate: drug effects
Histamine: pharmacology
Male
Morphine: pharmacology
Synaptic Transmission: drug effects
UCI Libraries Open Access Publishing Fund
article
Źródło :
Journal of NeuroEngineering and Rehabilitation vol 10, no 1, 111; 1743-0003
Wydawca :
eScholarship, University of California 2013-01-01
Dodane szczegóły :
Do, An H
Wang, Po T
King, Christine E
Chun, Sophia N
Nenadic, Zoran
Typ dokumentu :
Zasób elektroniczny
URL :
http://www.escholarship.org/uc/item/3tc1s456">http://www.escholarship.org/uc/item/3tc1s456
Dostępność :
Open access content. Open access content
Attribution (CC BY): http://creativecommons.org/licenses/by/3.0
Pozostałe numery :
CDLER qt3tc1s456
qt3tc1s456
1021973973
Źródło wspomagające :
UC MASS DIGITIZATION
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.on1021973973
Zasób elektroniczny
Neural ganglionic transmission was studied in vivo in the cat, using closed chest anesthetized preparations. The right stellate ganglion and its branches were exposed retropleurally and prepared for electrical stimulation of pre- and postganglionic nerve fibers. The axillary artery was cannulated allowing direct administration of drugs in the arterial blood supplying the ganglion. Stimulation of postjunctional receptors could thus be obtained by local administration of selective agents. Local administration of nicotinic, muscarinic or histaminergic agents increased heart rate and blood pressure. Opiates were given either i.v. or locally through the axillary artery: we tested the effects of morphine, Leu-enkephalin (Leu-enk), Met-enkephalin (Met-enk), [D-ala2]-Met-enkephalinamide (DAME) and etorphine. When given locally, Leu-enk (from 10 micrograms), Met-enk (from 20 micrograms), DAME (from 5 micrograms) and etorphine (from 0.2 micrograms) inhibited tachycardia induced by preganglionic stimulation and reduced the amplitude of the compound action potential recorded from the postganglionic nerve. Morphine (10-200 micrograms) had no effect. On the other hand, tachycardia induced by postganglionic nerve stimulation was unaffected by opiates in the same experimental conditions. Intravenous administration of similar doses of opiates had no effect on ganglionic transmission. When tachycardia was induced by chemical stimulation of nicotinic (DMPP), muscarinic (McN-A-343-11) or histamine receptors in the stellate ganglia, opiates were still active in reducing the effect of these chemicals. These data provide evidence that exogenous opiates exert a depressing action on postsynaptic responses of sympathetic ganglia tested in vivo, although an additional action on presynaptic terminals is not excluded. As endogenous opiates are normally present in various sympathetic ganglia, including the stellate ganglion of the cat, it is possible that they play some modulatory role on gangli

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